Dependence of chemotherapy response on p53 mutation status in a panel of human cancer lines maintained in nude mice

In contrast to findings in vitro, the clinical response to anticancer chemotherapy is not simply associated with the p53 mutation status. To analyze the relationship between the actual response of solid tumors with p53 mutation and other biological characteristics, we used a human cancer‐nude mouse...

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Bibliographic Details
Published in:Cancer science 2004-06, Vol.95 (6), p.541-546
Main Authors: Koike, Masako, Fujita, Fumiko, Komori, Kinuyo, Katoh, Fumitaka, Sugimoto, Takuji, Sakamoto, Yasuo, Matsuda, Masato, Fujita, Masahide
Format: Article
Language:English
Subjects:
5-Fluorouracil
Animals
Antineoplastic drugs
Antitumor agents
Apoptosis
Biological and medical sciences
Breast
Cancer
Cell Line, Tumor
Chemotherapy
Cisplatin
Cyclophosphamide
Deoxyribonucleic acid
DNA
DNA biosynthesis
DNA damage
Exons
Female
Genes, p53
Growth inhibition
Growth rate
Irinotecan
Male
Medical sciences
Mice
Mice, Nude
Mitomycin C
Mutants
Mutation
Neoplasm Transplantation
Neoplasms, Experimental - drug therapy
Neoplasms, Experimental - genetics
Neoplasms, Experimental - pathology
Nucleotide sequence
p53 Protein
Solid tumors
Transplantation, Heterologous
Tumors
Uracil
Xenografts
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Summary:In contrast to findings in vitro, the clinical response to anticancer chemotherapy is not simply associated with the p53 mutation status. To analyze the relationship between the actual response of solid tumors with p53 mutation and other biological characteristics, we used a human cancer‐nude mouse panel of 21 lines derived from stomach, colorectal, breast, lung, and liver cancers for experimental chemotherapy. We examined the tumor growth rates of the cancer lines and the effects of nine drugs in clinical use, namely, mitomycin C (MMC), cisplatin (CDDP), nimustine hydrochloride (ACNU), irinotecan (CPT‐11), cyclophosphamide (CPA), 1‐(2‐tetrahydrofuryl)‐5‐fluorouracil (FT‐207), a 4:1 mixture of uracil and FT‐207 (UFT), 5′‐deoxy‐5‐fluorouridine (5′‐DFUR), and adriamycin (ADM), on these tumors. The chemotherapy response was expressed as the tumor growth inhibition rate (IR). The genomic DNA sequences of the p53 gene in exons 5 through 8 were analyzed in these cancer tissues, and p53 mutations were detected in 10 of the 21 cancer lines (48%). Resistance to MMC was observed in p53 mutant tumors with smaller IRs than those for wild‐type tumors (57.7% vs. 79.9%, P
ISSN:1347-9032
1349-7006
DOI:10.1111/j.1349-7006.2004.tb03246.x